The landscape is vast, and much is obscured by mist. Some things are known, others knowable, perhaps still others, unknowable.
Science and patients as part of clinical trials, done formally or on their own, can push away some of the mist, bringing heretofore hidden details about chronic lymphocytic leukemia into the open, at last.

Friday, September 19, 2008

A lot has happened since my last post. I've been trying to get into the FCR+L trial since May, and I finally am supposed to start on Sunday, September 22, 2008. (There is a wrinkle; I've just developed a cough, so I need to have that checked out before I start the trial).

I was notified on Thursday that I have been randomized to be in the arm of the trial that includes the lumiliximab. Lumiliximab is a CD-23 antibody. It works in a fashion like rituximab, but the CD-23 marker isn't as good of a target.

The difference is that the CD-20 marker is a transmembrane protein; it pokes part of itself outside of the lymphocyte, and keeps the 'tail end' inside of the cell, in the cytoplasm I would assume. The way these markers work is they are the 'eyes and ears' of the cell, sensory organs if you will. The marker detects a signal outside of the cell in the microenvironment, and then signals inside of the cell.

Being a transmembrane molecule, the CD-2o marker is a robust one, hanging on the the cell (in large numbers, in the thousands), resisting falling off and becoming useless. The CD-23 marker, unlike the CD-20, is much more easily dislodged from the cell, and a detectable fraction of the markers are found in the microenvironment. This makes the CD-23 marker less effective at killing CLL cells.

The hope the company who is pushing this MoAB through clinical trials is that it will enhance standard therapies. Small studies have suggested that this is true; the complete remission rate with FCR+L is higher than plain old FCR.

I am scheduled to start the study this coming week at the University of California, Davis Medical Center. Although I've gotten all of my treatment so far from UC San Diego, I opted for UCD this time because the trial protocol they offered me allowed either MRIs or CT scans. Anyone who knows me knows that I dislike CT scans because of the amount of radiation, which raises the risk of secondary malignancies, a complication CLL patients are already at higher risk for.

The secondary reason is that I live in Sacramento, and this will mean not having to fly down to San Diego for follow-up visits and all six cycles, assuming I would get that far.

As far as my general health goes, I am fading, but not at a fast clip. My biggest problem is my anemia. I am in the 8.8 range at last test, and this is not normal. Even the government will pay for Epogen if the hemo rate is below 10.0, which I am.

My other numbers are terrible, but sort of holding steady. WBC at the 200,000 range, platelets (always a problem for me) at about 75, and the red blood counts, as I've mentioned, a continuing problem.

My latest test should be on my fax machine when I get home tonight, so I should know if I need a transfusion in the next day or two.

My biggest problem right now is this cough I can't get rid of. Dr. Hamblin believes I should wait before I start the trial, and I am inclined to agree with him.

I think I got this latest infection (I've been remarkably infection-free even with terrible numbers, until this year, and I've had three infections since January) from using a neti pot. This is a device that allows you to pour salt water from one nostril into the other, draining stuff and supposedly keeping you clean. However, I made the mistake of just using tap water, which is not sterile. I usually boil the water, but just forgot.